Evaluation of experimental myocardial infarction models via electromechanical mapping and magnetic resonance imaging.

The diagnostic characteristics of electromechanical mapping (EMM) were evaluated in porcine myocardial infarction (MI) models with the parallel application of cardiac magnetic resonance imaging (cMRI) from the aspect of different pathophysiology and localization. Balloon occlusion in the left anterior descending coronary artery (LAD balloon group) or coil deployment in the LAD (LAD coil group) or circumflex artery (Cx coil group) was applied percutaneously in 16 domestic pigs. Regional left ventricular viability data were captured via cMRI and EMM. The unipolar voltage (UV) value was significantly decreased in segments containing transmural and subendocardial late enhancement compared with viable segments in the LAD balloon, LAD coil, and Cx coil groups. Receiver operating characteristic analysis revealed area under the curve values of 0.809 and 0.691 in the LAD infarct territory, and 0.864 and 0.855 in the Cx infarct territory for the UV compared with cMRI viability results as transmural late enhancement or viable tissue and subendocardial late enhancement or viable tissue, respectively. In conclusion, the UV value detected the presence of scar tissue with differential transmural extent and which represented proper diagnostic features both in the reperfused and nonreperfused models. This data could provide additional benefit in the clinical use of EMM for diagnostic purposes.

Intraamygdaloid microinjection of acylated-ghrelin influences passive avoidance learning.

The brain-gut peptide acylated-ghrelin (A-Ghr) is a potent growth hormone (GH) secretagogue substance. A-Ghr is also known to influence on memory and learning processes. Its effect is mediated partly via GH secretagogue receptor (GHS-R) type 1a. The amygdaloid body (AMY) plays important role in memory and learning processes. Projections of ghrelinergic neurons were identified in the AMY, and previously we verified that A-Ghr infused into basolateral nucleus of the AMY (ABL) caused liquid food intake decrease. The aim of the present study was to examine the possible effects of A-Ghr in the ABL on learning. Male Wistar rats were examined in two-compartment passive avoidance paradigm. Animals were shocked with 0.4mA current and subsequently were microinjected bilaterally with 50 or 100 ng A-Ghr, 30 ng GHS-R antagonist d-Lys3-GHRP-6 (ANT), ANT+50 ng A-Ghr (dissolved in 0.15M sterile NaCl/0.4 microl) or vehicle into the ABL. Fifty nanogram A-Ghr significantly increased the latency time, the 100 ng and the ANT alone were ineffective. The effect of 50 ng A-Ghr was eliminated by the ANT pretreatment. Our results suggest that intraamygdaloid A-Ghr enhances learning processes and memory in aversive situations, and this effect can specifically be prevented by ANT pretreatment.

Effects of intraamygdaloid microinjections of acylated-ghrelin on liquid food intake of rats.

Ghrelin (Ghr) has two main forms in the blood: the acylated (A-Ghr) and non-acylated (NA-Ghr) Ghr. A-Ghr was discovered as a potent growth hormone (GH) secretion increasing substance acting on GH secretagouge receptor (GHS-R) type 1a. A-Ghr facilitates food intake after its i.p., i.c.v. or direct hypothalamic application. Immunohistological assays identified projections of ghrelinergic neurons to the basolateral nucleus (ABL) of the amygdala (AMY). A-Ghr injected into the hypothalamus caused c-Fos overexpression in the AMY area that has an important role in food intake and body weight regulation. In separate experiments, liquid food intake of male wistar rats was measured after bilateral intraamygdalar or bilateral i.c.v. administration of A-Ghr (25, 50, 100, 250, and 500 ng/side or 500 and 1000 ng/side, A-Ghr dissolved in 0.15 M sterile NaCl/0.4 microl or 1 microl, respectively). In the ABL, A-Ghr microinjections in the 50-250 ng dose range resulted in significant decrease of food intake. The 25 and 500 ng had no effect. Action of 50 ng (14.83 pmol) or 100 ng (30.16 pmol) A-Ghr was eliminated by 15 ng (16.13 pmol) or 30 ng (32.25 pmol) GHS-R antagonist (D-Lys3-GHRP-6) pretreatment. The administration of 30 ng D-Lys3-GHRP-6 in itself had no influence on feeding. I.c.v. applied 1000 ng A-Ghr increased liquid food intake. Our results are the first ones reporting that A-Ghr injected into the ABL resulted in a decrease of liquid food consumption, within a limited dose range. This is a receptor-linked effect because it was eliminated by a GHS-R specific antagonist.